pre-existing conditions Flashcards
(45 cards)
pregestational and gestational diabetes
hyperglycemia resulting from defects in insulin secretion, insulin action, or both. pregestational diabetes is diabetes 1 (B-cell destruction in pancreas) or 2 (insulin resistance or deficiency) that was present in women before pregnancy. gestational diabetes is women who have carbohydrate intolerance discovered during pregnancy - any degree of glucose intolerance with onset or recognition during pregnancy; applies whether insulin used for treatment or diabetes persists after pregnancy. Women who experience gestational diabetes should be followed up with 6 weeks and 6 months after birth for presence of underlying disease
signs of diabetes in pregnancy
polyuria - large volumes of urine due to kidney excreting excess blood volume from hyperglycemia (hyperglycemia causes hyperosmolarity where intracellular fluid gets pulled into the vascular system to dilute the glucose concentration)
glycosuria - glucose in the urine
polydipsia - excessive thirst due to polyuria and cellular dehydration
polyphagia - excessive hunger caused by starvation due to tissue breakdown of fats and muscles for energy to compensate for inability of body to convert carbs (glucose) into energy
two insulin conditions in diabetes
impaired insulin secretion due to beta cells of the pancreas being destroyed by an autoimmune process
inadequate insulin action in target tissues at one or more points along the metabolic pathway
- both these conditions present in same person, difficult to determine which abnormality is primary
normal glucose cycle in pregnancy
glucose, primary fuel used by the fetus, is transported across the placenta through diffusion, thus glucose level in fetus directly proportional to maternal glucose level. Glucose crosses the placenta but insulin does not so around the 10th week the fetus secretes its own insulin level to match the glucose level crossing the placenta. in first and second trimester Estrogen and progesterone (pregnancy hormones) stimulate the B-cells in the pancreas to increase insulin production; increasing peripheral use of glucose and decreasing blood glucose. At the same time increases in tissue glycogen stores and decrease in hepatic glucose production lower fasting glucose. During latter part of second and all through third trimester pregnancy exerts a diabetogenic effect, decreasing tolerance of glucose, increasing insulin resistance, decreasing hepatic stores, and increasing hepatic production of glucose. insulin resistance is a glucose sparing mechanism to ensure enough glucose for the fetus. Insulin requirements increase from 18 or 24 weeks to 36 weeks where it levels out. at birth the expulsion of the placenta prompts an abrupt decrease in pregnancy hormones, cortisol, and insulinase. maternal tissue quickly regains its prepregnancy sensitivity to insulin. for non breastfeeding it prepregnancy insulin-carb balance restored in 7 to 10 days. in breastfeeding insulin requirement remains low until infant weaned.
pregestational diabetes and glucose levels in pregnancy
due to low glucose level as natural part of first and second trimester women with pregestational diabetes tend to be hypoglycemic. women with diabetes require insulin throughout pregnancy. Hormonal changes in pregnancy that affect glycemic control may accelerate vascular complications of diabetes. During first semester when blood glucose is low and insulin response to glucose is enhanced there is better glycemic control. Insulin dose must be adjusted during pregnancy for rising insulin resistance in second and third trimester (more insulin needed) and and hypoglycemia in first and second trimester (less insulin needed).
preconception counselling for diabetic women
strict metabolic control important to reduce congenital anomalies and spontaneous abortion during organogenesis in early weeks of pregnancy. use of oral antihyperglycemic meds alone in pregnancy not recommended.
Maternal risks with diabetes in pregnancy
risk factors include blood glucose control, length of time since diagnosis, and existing diabetic complications present. women with pregestational diabetes who have poor glycemic control (defined as glycosylated hemoglobin value greater than 7.0% around time of conception and in early pregnancy) have twofold increased incidence of early pregnancy loss. Poor glycemic control later in pregnancy increase the rate of fetal macrosomia (birth weight more than 400-4500g). assessment for retinopathy recommended in preconception, during first trimester, as needed throughout pregnancy, and 1 year postpartum. Hydramnios (Amniotic fluid index (AFI) greater than 24 and 25cm) frequently develop during third trimester of woman with diabetes thought to result from increase glucose concentration in amniotic fluid from maternal and fetal hyperglycemia.
infection in diabetic pregnant woman
disorder of carbohydrate metabolism alter body’s normal resistance to infection - inflammation response, leukocyte function, and vaginal pH all affected. infection may cause insulin resistance resulting in ketoacidosis. postpartum infection more likely to occur in woman with poor glycemic control. Most common concern in pregnancy is loss of hypoglycemic awareness - more common in long standing diabetes and safety concern for mothers- hypoglycemic awareness may return after pregnancy.
ketoacidosis in pregnancy
build up of ketones in the blood due to hyperglycemia - the body breaks down fat too fast to accommodate for energy demands and releases ketones into the blood making it more acidic; leads to metabolic acidosis. occurs most often during second and third trimester when diabetogenic effect is greatest. DKA occur due to over or under administration of insulin. DKA occur with blood glucose levels barely exceeding 11 mmol/L because of increase in the body’s resistance to insulin. Excessive blood glucose and ketones results in osmotic diuresis with subsequent loss of fluids and electrolytes, volume depletion, and cellular dehydration.
Hypoglycemia in diabetic pregnancy
less than normal amount of glucose in the blood. Abnormal postnatal neurological development occurs when long term hypoglycemia results in ketosis (break down of fat or muscle to meet energy demands not provided by carbs - glucose)
fetal and neonatal risks with diabetes
stillbirth significant risk. in third trimester fetal acidosis is most likely cause of death. most important cause of perinatal loss is congenital malformation - incidence of malformations directly related to severity and duration of diabetes. Hyperglycemia during organogenesis main cause of birth defects. Morbidity and mortality of fetal reduce with strict maternal glycemic control before and during pregnancy. Macrosomia due to increased insulin secretion (hyperinsulinism) to accommodate hyperglycemia acting as a growth hormone. Hypoglycemia also risk for infants depending on glycemic control of mother in last trimester of pregnancy (increased insulin demands)
insulin shock (hypoglycemia) in pregnancy
due to: excess insulin, insufficient food (delayed or missed meals), excessive excersize or work, indigestion (vomiting or diarrhea). Rapid onset for regular insulin or gradual onset for modified insulin or oral hypoglycemic agents. s&s: hunger, blurred vision, personality changes,
interventions for insulin shock in pregnancy
check blood glucose levels, eat 15g of fast sugar, recheck blood glucose in 15min and eat another 15g fast sugar if low, recheck blood glucose in 15min again, notify healthcare provider if no change in blood glucose level. If woman unconscious admin 50% dextrose IV push, 50 to 10% dextrose in water IV drip, or 1 mg glucagon subQ. obtain blood and urine specimen for lab testing
diabetic ketoacidosis (hyperglycemia) in pregnancy
due to: insufficient insulin, excess or wrong kind of food, infection, injury, or illness, emotional stress, insufficient excersize. Slow onset (hours to days). S&S: thirst, abdominal pain, acetone (fruity) breath odour
interventions for DKA in pregnancy
notify healthcare provider, admin insulin in accordance with blood glucose levels, give IV fluids such as normal saline solution or one half normal saline solution; potassium when urinary output adequate; bicarbonate for pH <7, monitor laboratory testing of blood and urine
hyperthyroidism in pregnancy
most commonly caused by graves disease or human chorionic gonadotropin (hCG) mediated hyperthyroidism. symptoms generally begin 4 to 8 weeks of gestation and involve severe nausea and vomiting. dx: thyroid levels in blood. woman with minimal or mild symptoms - low thyroid stimulating hormone and mild elevated thyroxine - can be monitored without intervention. Signs to differentiate mild from severe hyperthyroidism include unplanned weight loss, loose nails, and HR 100bpm/min or higher. two primary meds to treat hyperthyroidism in pregnancy; propylthiouracil (PTU) and methimazole (MM). MM has teratogenic effects so is avoided in first trimester, PTU is associated with liver failure so only used in first trimester to prevent toxicity. Thyroid function test performed 2 to 4 weeks after switch from PTU to MM to be sure euthyroid maintained. Beta adrenergic blockers used for severe symptoms but not long term due to adverse effects on postnatal bradycardia, anoxic stress, hypoglycemia, and IUGR. med can be passed through breastfeeding so a breastfeeding newborn thyroid function should be monitored periodically to prevent hypothyroidism. In severe cases, hyperthyroidism can be surgically dealt with by removing the thyroid (subtotal thyroidectomy) in second or third trimester.
thyroid storm in pregnancy
uncommon but serious complication of untreated or partially treated hyperthyroidism. it occurs in response to stresses such as severe pre-eclampsia, infection, birth or surgery. Prompt treatment with PTU, IV fluids, and oxygen required. Potassium iodide, antipyretics, glucocorticoids, and beta adrenergic blockers may also be given; sedation may be necessary. symptoms include sudden fever, tachycardia, restlessness, vomiting, hypotension, or stupor. HF also may occur
hypothyroidism in pregnancy
TSH levels high caused by underactive thyroid. most common cause of thyroid problems is iodine deficiency. signs of hypothyroidism include cool and dry skin, weight gain, coarsened hair, muscle weakness, cold intolerance, decrease in excersize capacity, constipation, and fatigue. hypothyroidism shown to cause neurological development impairment in early fetal development. fetus dependent on maternal transfer of thyroid hormones for first 18 weeks of pregnancy, specifically T4 - if mother deficient, fetal brain cannot develop properly. Thyroid hormone supplement treatment of choice, specifically levothyroxine as it is not a teratogenic. Thyroid hormone treatment must be adjustment for demand throughout pregnancy (demand generally goes up as pregnancy progresses). Take meds on empty stomach for increased absorption and take prenatal vitamins 4 hours after thyroid hormones as iron and calcium affect absorption of hormone.
Maternal cardiac disease risk group 1
mortality rate <1% ASD and VSD PDA corrected tetralogy of fallot pulmonic/tricuspid disease mitral stenosis or aortic regurgitation bioprosthetic valve mitral valve prolapsed with regurgitation
maternal cardiac disease risk group 2
mortality rate 5-20% aortic stenosis coarctation of the aorta without valve involvement artificial heart valves mitral stenosis or with atrial fibrillation uncorrected tetralogy of fallot previous myocardial infarction marfan syndrome with normal aorta
maternal cardiac disease risk group 3
mortality rate 25-50%
pulmonary hypertension
coarctation of the aorta with valvular involvement
complicated marfan syndrome with aortic involvement
endocarditis
eisenmenger syndrome
peripartum cardiomyopathy with persistent left ventricular dysfunction
Cardiovascular disorders in pregnancy
changes that occur in pregnancy that affect women with cardiac disease are increased vascular volume, decreased systemic vascular resistance, cardiac output changes in labour, and intravascular changes that occur just after birth
if myocardial disease develops, valvular disease exists, or congenital heart defect is present, cardiac decompensation (inability of the heart to maintain a sufficient cardiac output) may occur
Fever and infection major causes of cardiac decompensation in pregnancy
New York Heart Association (NYHA) functional classification of heart disease
Class I: asymptomatic without limitation of physical activity
Class II: symptomatic with slight limitation of activity
Class III: symptomatic with marked limitation of activity
Class IV: symptomatic with inability to carry out activity without discomfort
note: woman assessed for classification at 3 months and then again at 7 or 8 months
congenital cardiac disease in pregnancy
women at risk for cardiac event in pregnancy include those with a prior cardiac event, arrhythmia, NYHA functional class greater than II, cyanosis, left heart obstruction, and systemic ventricular dysfunction
